About: Cytokine and Chemokine Profiles in Lung Tissues from Fatal Cases of 2009 Pandemic Influenza A (H1N1) Role of the Host Immune Response in Pathogenesis

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About: Cytokine and Chemokine Profiles in Lung Tissues from Fatal Cases of 2009 Pandemic Influenza A (H1N1) Role of the Host Immune Response in Pathogenesis Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Cytokine and Chemokine Profiles in Lung Tissues from Fatal Cases of 2009 Pandemic Influenza A (H1N1) Role of the Host Immune Response in Pathogenesis
Creator	Sambhara, Suryaprakash Gao, Rongbao Shu, Yuelong Zaki, Sherif Shieh, Wun-Ju Liu, Lindy Blau, Dianna Paddock, Christopher Bhatnagar, Julu Deleon-Carnes, Marlene Drew, Clifton Greer, Patricia Patel, Mitesh Katz, Jacqueline Tumpey, Terrence Denison, Amy Rollin, Dominique
Source	Elsevier; Medline; PMC
abstract	Pathological studies on fatal cases caused by 2009 pandemic influenza H1N1 virus (2009 pH1N1) reported extensive diffuse alveolar damage and virus infection predominantly in the lung parenchyma. However, the host immune response after severe 2009 pH1N1 infection is poorly understood. Herein, we investigated viral load, the immune response, and apoptosis in lung tissues from 50 fatal cases with 2009 pH1N1 virus infection. The results suggested that 7 of the 27 cytokines/chemokines showed remarkably high expression, including IL-1 receptor antagonist protein, IL-6, tumor necrosis factor-α, IL-8, monocyte chemoattractant protein-1, macrophage inflammatory protein 1-β, and interferon-inducible protein-10 in lung tissues of 2009 pH1N1 fatal cases. Viral load, which showed the highest level on day 7 of illness onset and persisted until day 17 of illness, was positively correlated with mRNA levels of IL-1 receptor antagonist protein, monocyte chemoattractant protein-1, macrophage inflammatory protein 1-β, interferon-inducible protein-10, and regulated on activation normal T-cell expressed and secreted. Apoptosis was evident in lung tissues stained by the TUNEL assay. Decreased Fas and elevated FasL mRNA levels were present in lung tissues, and cleaved caspase-3 was frequently seen in pneumocytes, submucosal glands, and lymphoid tissues. The pathogenesis of the 2009 pH1N1 virus infection is associated with viral replication and production of proinflammatory mediators. FasL and caspase-3 are involved in the pathway of 2009 pH1N1 virus-induced apoptosis in lung tissues, and the disequilibrium between the Fas and FasL level in lung tissues could contribute to delayed clearance of the virus and subsequent pathological damages.
has issue date	2013-10-31(xsd:dateTime)
bibo:doi	10.1016/j.ajpath.2013.06.023
bibo:pmid	23938324
has license	els-covid
sha1sum (hex)	b18702fc4d911dbdff97f9ae5a4020e9a93bb80c
schema:url	https://doi.org/10.1016/j.ajpath.2013.06.023
resource representing a document's title	Cytokine and Chemokine Profiles in Lung Tissues from Fatal Cases of 2009 Pandemic Influenza A (H1N1) Role of the Host Immune Response in Pathogenesis
has PubMed Central identifier	PMC7119452
has PubMed identifier	23938324
schema:publication	The American Journal of Pathology
resource representing a document's body	covid:b18702fc4d911dbdff97f9ae5a4020e9a93bb80c#body_text
is schema:about of	named entity 'FATAL' named entity 'Pathogenesis' named entity 'Cytokine' named entity 'HOST IMMUNE RESPONSE' named entity 'CHEMOKINE' named entity 'INFLUENZA A' named entity 'CASES' named entity 'ROLE' named entity 'PANDEMIC' named entity 'PATHOGENESIS' named entity 'LUNG TISSUES' named entity 'CYTOKINE ' named entity 'Cytokine' named entity 'IL-1RA' named entity 'pH1N1' named entity 'caspase-3' named entity 'pneumocytes' named entity 'cytokine' named entity 'FasL' named entity 'Histopathological' named entity 'American Journal of Pathology' named entity 'chemokine' named entity 'influenza' named entity 'TNF-a' named entity 'lung parenchyma' named entity 'Bio-Rad' named entity 'Cell Death' named entity 'S. pyogenes' named entity 'morbidity' named entity 'IL-6' named entity 'lung tissue' named entity 'IL-6' named entity 'IL-8' named entity 'IL-1RA' named entity 'viral load' named entity 'Roche' named entity 'formalin' named entity 'IP-10' named entity 'lungs' named entity 'nasopharyngeal' named entity 'two-tailed test' named entity 'viral load' named entity 'IL-8' named entity 'Tcell' named entity 'basic fibroblast growth factor' named entity 'tumor necrosis factor' named entity 'lysed' named entity 'positively correlated' named entity 'RT-qPCR' named entity 'Agilent Technologies Inc.' named entity 'Haemophilus influenzae' named entity 'virus' named entity 'morbidity' named entity 'viral load' named entity 'immune response' named entity 'antibodies' named entity 'IL-6' named entity 'cytokines' named entity 'influenza' named entity 'Viral pathogenesis' named entity 'TNF-a' named entity 'Viral load' named entity 'IL-6' named entity '50 million' named entity 'middle-aged'

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